Moderate versus severe early life stress: Associations with stress reactivity and regulation in 10–12-year-old children (original) (raw)

Maternal stress beginning in infancy may sensitize children to later stress exposure: effects on cortisol and behavior

Biological Psychiatry, 2002

Background: Preclinical studies demonstrate that the neonatal environment can permanently alter an individual's responses to stress. To demonstrate a similar phenomenon in humans, we prospectively examined the relationships of maternal stress beginning in infancy and concurrent stress on preschoolers' hypothalamic-pituitary-adrenal activity and later mental health symptoms. Methods: Salivary cortisol levels were assessed in 282 4.5-year-old children and 154 of their siblings. Maternal reports of stress were obtained when the children were ages 1, 4, and 12 months, and again at 4.5 years. Children's mental health symptoms were assessed in first grade. Results: A cross-sectional analysis revealed that preschoolers exposed to high levels of concurrent maternal stress had elevated cortisol levels; however, a longitudinal analysis revealed that concurrently stressed children with elevated cortisol also had a history of high maternal stress exposure in infancy. Importantly, children exposed only to high levels of concurrent or early stress had cortisol levels that did not significantly differ from those never exposed to stress. Further analysis of the components of stress indicated that maternal depression beginning in infancy was the most potent predictor of children's cortisol. We also found that preschoolers with high cortisol levels exhibited greater mental health symptoms in first grade. Conclusions: These results link the findings of preclinical studies to humans by showing that exposure to early maternal stress may sensitize children's pituitary-adrenal responses to subsequent stress exposure. Biol Psychiatry 2002;52:776 -784

Early deprivation and home basal cortisol levels: A study of internationally adopted children

Development and Psychopathology, 2008

Animal studies reveal that early deprivation impairs regulation of the hypothalamic-pituitary-adrenocortical (HPA) axis, potentially increasing vulnerability to stressors throughout life. To examine early deprivation effects on basal HPA axis activity in humans, basal cortisol levels were examined in 164 internationally adopted children who had experienced varying degrees of preadoption deprivation. Duration of institutional care, age at adoption, and parent ratings of preadoption neglect indexed a latent factor of Deprived Care. Adoption measures of height and weight standardized to World Health Organisation norms indexed a latent factor of Growth Delay that was viewed as another reflection of deprivation. Cortisol samples were collected 3.3-11.6 years postadoption (Md ¼ 7.3 years) at home on 3 days approximately 30 min after wakeup and before bedtime. Both early a.m. levels and the decrease in cortisol across the day were examined. A structural equation model revealed that preadoption Deprived Care predicted Growth Delay at adoption and Growth Delay predicted higher morning cortisol levels and a larger diurnal cortisol decrease.

Stress physiology and developmental psychopathology: Past, present, and future

Research on the hypothalamic–pituitary–adrenocortical (HPA) axis has emerged as a vital area within the field of developmental psychopathology in the past 25 years. Extensive animal research has provided knowledge of the substrates and physiological mechanisms that guide development of stress reactivity and regulation using methods that are not feasible in humans. Recent advances in understanding the anatomy and physiology of the HPA axis in humans and its interactions with other stress-mediating systems, including accurate assessment of salivary cortisol, more sophisticated neuroimaging methods, and a variety of genetic analyses, have led to greater knowledge of how psychological and biological processes impact functioning. A growing body of research on HPA axis regulation and reactivity in relation to psychopathology has drawn increased focus on the prenatal period, infancy, and the pubertal transition as potentially sensitive periods of stress system development in children. Theories such as the allostatic load model have guided research by integrating multiple physiological systems and mechanisms by which stress can affect mental and physical health. However, almost none of the prominent theoretical models in stress physiology are truly developmental, and future work must incorporate how systems interact with the environment across the life span in normal and atypical development. Our theoretical advancement will depend on our ability to integrate biological and psychological models. Researchers are increasingly realizing the importance of communication across disciplinary boundaries in order to understand how experiences influence neurobehavioral development. It is important that knowledge gained over the past 25 years has been translated to prevention and treatment interventions, and we look forward to the dissemination of interventions that promote recovery from adversity.

Interactive effects of early and recent exposure to stressful contexts on cortisol reactivity in middle childhood

2014

Background: Given mixed findings as to whether stressful experiences and relationships are associated with increases or decreases in children's cortisol reactivity, we tested whether a child's developmental history of risk exposure explained variation in cortisol reactivity to an experimentally induced task. We also tested whether the relationship between cortisol reactivity and children's internalizing and externalizing problems varied as a function of their developmental history of stressful experiences and relationships. Method: Participants included 400 children (M = 9.99 years, SD = 0.74 years) from the Children's Experiences and Development Study. Early risk exposure was measured by children's experiences of harsh, nonresponsive parenting at 3 years. Recent risk exposure was measured by children's exposure to traumatic events in the past year. Children's cortisol reactivity was measured in response to a social provocation task and parents and teachers described children's internalizing and externalizing problems. Results: The effect of recent exposure to traumatic events was partially dependent upon a child's early experiences of harsh, nonresponsive parenting: the more traumatic events children had recently experienced, the greater their cortisol reactivity if they had experienced lower (but not higher) levels of harsh, nonresponsive parenting at age 3. The lowest levels of cortisol reactivity were observed among children who had experienced the most traumatic events in the past year and higher (vs. lower) levels of harsh, nonresponsive parenting in early childhood. Among youth who experienced harsh, nonresponsive parent-child relationships in early childhood and later traumatic events, lower levels of cortisol reactivity were associated with higher levels of internalizing and externalizing problems. Conclusions: Hypothalamic-pituitary-adrenal (HPA) axis reactivity to psychological stressors and the relationship between HPA axis reactivity and children's internalizing and externalizing problems vary as a function of a child's developmental history of exposure to stressful relationships and experiences.

The symphonic structure of childhood stress reactivity: Patterns of sympathetic, parasympathetic, and adrenocortical responses to psychological challenge

Development and Psychopathology, 2014

Despite widespread recognition that the physiological systems underlying stress reactivity are well coordinated at a neurobiological level, surprisingly little empirical attention has been given to delineating precisely how the systems actually interact with one another when confronted with stress. We examined crosssystem response proclivities in anticipation of and following standardized laboratory challenges in 664 4-to 14-year-olds from four independent studies. In each study, measures of stress reactivity within both the locus coeruleus-norepinephrine system (i.e., the sympathetic and parasympathetic branches of the autonomic nervous system) and the corticotrophin releasing hormone system (i.e., the hypothalamic-pituitary-adrenal axis) were collected. Latent profile analyses revealed six distinctive patterns that recurred across the samples: moderate reactivity (average cross-system activation; 52%-80% of children across samples), parasympathetic-specific reactivity (2%-36%), anticipatory arousal (4%-9%), multisystem reactivity (7%-14%), hypothalamic-pituitary-adrenal axis specific reactivity (6%-7%), and underarousal (0%-2%). Groups meaningfully differed in socioeconomic status, family adversity, and age. Results highlight the sample-level reliability of children's neuroendocrine responses to stress and suggest important cross-system regularities that are linked to development and prior experiences and may have implications for subsequent physical and mental morbidity.

Timing matters: Long term effects of adversities from prenatal period up to adolescence on adolescents’ cortisol stress response. The TRAILS study

Psychoneuroendocrinology, 2012

Objective: Altered cortisol response is a vulnerability marker for a variety of stress-related diseases and psychiatric disorders. Childhood adversity has been shown to modify this response, but evidence is inconsistent. Effects may differ depending on the timing of exposure, or due to the interplay between pre/postnatal adversity and later adversities. The present study examined the influence of adversity during different timeframes (pre/postnatal, ages 0-5, 6-11, 12-13, 14-15 years), and the interaction between pre/postnatal and later adversity on adolescents' cortisol stress response. Method: Four salivary cortisol samples were collected before and after a social stress test in 471 16-year-old adolescents from the longitudinal study TRAILS. Data on pre/postnatal exposure to adversities were obtained from Preventive Child Healthcare records and parental reports, subsequent adversities from parental and self-reports. Results: Pre/postnatal adversity was associated with increased cortisol reactivity. Adversities during ages 0-5 were not associated with cortisol outcomes. Adversities during ages 6-11

Stress system development from age 4.5 to 6: Family environment predictors and adjustment implications of HPA activity stability versus change

Developmental Psychobiology, 2014

This study addressed early calibration of stress systems by testing links between adversity exposure, developmental stability of hypothalamic-pituitary-adrenal (HPA) axis activity, and behavior problems in a sample of adopted children. Families (n=200) were assessed when the child was 9mos, 18mos, 27mos, 4.5yrs, and 6yrs to collect adversity information-parent psychopathology, stress, financial need, and home chaos. Morning and evening cortisol samples at the final 2 assessments indexed child HPA activity, and parent-reported internalizing and externalizing at the final assessment represented child behavior outcomes. Increases in cumulative adversity from 4.5-6 related to higher child morning cortisol, whereas age 6 cumulative adversity related to lower, unstable child evening cortisol. Examination of specific adversity dimensions revealed associations between (1) increasing home chaos and stable morning cortisol, which in turn related to internalizing problems; and (2) high parental stress and psychopathology and lower, unstable evening cortisol, which in turn related to externalizing problems.

Stress and development: Behavioral and biological consequences

Development and Psychopathology, 2001

Childhood abuse is an important public health problem; however, little is known about the effects of abuse on the brain and neurobiological development. This article reviews the behavioral and biological consequences of childhood abuse and places them in a developmental context. Animal studies show that both positive and negative events early in life can influence neurobiological development in unique ways. Early stressors such as maternal separation result in lasting effects on stress-responsive neurobiological systems, including the hypothalamic-pituitary-adrenal (HPA) axis and noradrenergic systems. These studies also implicate a brain area involved in learning and memory, the hippocampus, in the long-term consequences of early stress. Clinical studies of patients with a history of abuse also implicate dysfunction in the HPA axis and the noradrenergic and hippocampal systems; however, there are multiple questions related to chronicity of stress, developmental epoch at the time of the stressor, presence of stress-related psychiatric disorders including posttraumatic stress disorder and depression, and psychological factors mediating the response to trauma that need to be addressed in this field of research. Understanding the effects of abuse on the development of the brain and neurobiology will nevertheless have important treatment and policy implications.

Altered stress responses in children exposed to early adversity: a systematic review of salivary cortisol studies

Stress (Amsterdam, Netherlands), 2011

Pathological stress responses are implicated in numerous disorders. Hypothalamic-pituitary-adrenal axis function is influenced by gene-environment interaction, with early-life environmental adversity having long-lasting effects. We examine the evidence that, in humans, these effects are apparent from infancy. We systematically reviewed published findings on cortisol response to a stressor, in 0-5-year-olds already exposed to adversity. Adversity was defined as a negative environmental influence present post-conception. We searched Ovid MEDLINE (1950-May 2010), EMBASE (1980-May 2010) and PsychINFO (1806-May 2010). We included peer-reviewed, English language studies that analysed salivary cortisol before and after a standardised stressor. We identified 30 studies, of which 27 reported a significant effect of adversity on the cortisol response to stress. Six of these demonstrated an effect of prenatal substance exposure. Thirteen studies found that psychosocial adversity increased cort...